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Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets?
BACKGROUND: Hypercapnia causes cerebral vasodilation and increased cerebral blood flow (CBF). During prolonged hypercapnia it is unknown whether cerebral vasodilation persists and whether cerebrovascular function is preserved. We investigated the effects of prolonged severe hypercapnia on pial arter...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6185793/ https://www.ncbi.nlm.nih.gov/pubmed/29907849 http://dx.doi.org/10.1038/s41390-018-0061-5 |
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author | Pourcyrous, Massroor Chilakala, Sandeep Elabiad, Mohamad T Parfenova, Helena Leffler, Charles W |
author_facet | Pourcyrous, Massroor Chilakala, Sandeep Elabiad, Mohamad T Parfenova, Helena Leffler, Charles W |
author_sort | Pourcyrous, Massroor |
collection | PubMed |
description | BACKGROUND: Hypercapnia causes cerebral vasodilation and increased cerebral blood flow (CBF). During prolonged hypercapnia it is unknown whether cerebral vasodilation persists and whether cerebrovascular function is preserved. We investigated the effects of prolonged severe hypercapnia on pial arteriolar diameters (PAD) and cerebrovascular reactivity to vasodilators and vasoconstrictors. METHODS: Piglets were anesthetized, intubated and ventilated. Closed cranial windows were implanted to measure PAD. Changes in PAD were documented during hypercapnia (PaCO(2) 75–80 mm Hg). Cerebrovascular reactivity was documented during normocapnia and at 30, 60 and 120 min of hypercapnia. RESULTS: Cerebral vasodilation to hypercapnia was sustained over 120 min. Cerebrovascular responses to vasodilators and vasoconstrictors were preserved during hypercapnia. During hypercapnia, vasodilatory responses to second vasodilators were similar to normocapnia, while exposure to vasoconstrictors caused significant vasoconstriction. CONCLUSIONS: Prolonged severe hypercapnia causes sustained vasodilation of pial arteriolar diameters indicative of hyperperfusion. During hypercapnia, cerebral vascular responses to vasodilators and vasoconstrictors were preserved, suggesting that cerebral vascular function remained intact. Of note, cerebral vessels during hypercapnia were capable of further dilation when exposed to additional cerebral vasodilators and, significant vasoconstriction when exposed to vasoconstrictors. Extrapolating these findings to infants, we suggest that severe hypercapnia should be avoided, because it could cause/increase cerebrovascular injury. |
format | Online Article Text |
id | pubmed-6185793 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
record_format | MEDLINE/PubMed |
spelling | pubmed-61857932018-11-28 Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? Pourcyrous, Massroor Chilakala, Sandeep Elabiad, Mohamad T Parfenova, Helena Leffler, Charles W Pediatr Res Article BACKGROUND: Hypercapnia causes cerebral vasodilation and increased cerebral blood flow (CBF). During prolonged hypercapnia it is unknown whether cerebral vasodilation persists and whether cerebrovascular function is preserved. We investigated the effects of prolonged severe hypercapnia on pial arteriolar diameters (PAD) and cerebrovascular reactivity to vasodilators and vasoconstrictors. METHODS: Piglets were anesthetized, intubated and ventilated. Closed cranial windows were implanted to measure PAD. Changes in PAD were documented during hypercapnia (PaCO(2) 75–80 mm Hg). Cerebrovascular reactivity was documented during normocapnia and at 30, 60 and 120 min of hypercapnia. RESULTS: Cerebral vasodilation to hypercapnia was sustained over 120 min. Cerebrovascular responses to vasodilators and vasoconstrictors were preserved during hypercapnia. During hypercapnia, vasodilatory responses to second vasodilators were similar to normocapnia, while exposure to vasoconstrictors caused significant vasoconstriction. CONCLUSIONS: Prolonged severe hypercapnia causes sustained vasodilation of pial arteriolar diameters indicative of hyperperfusion. During hypercapnia, cerebral vascular responses to vasodilators and vasoconstrictors were preserved, suggesting that cerebral vascular function remained intact. Of note, cerebral vessels during hypercapnia were capable of further dilation when exposed to additional cerebral vasodilators and, significant vasoconstriction when exposed to vasoconstrictors. Extrapolating these findings to infants, we suggest that severe hypercapnia should be avoided, because it could cause/increase cerebrovascular injury. 2018-05-28 2018-08 /pmc/articles/PMC6185793/ /pubmed/29907849 http://dx.doi.org/10.1038/s41390-018-0061-5 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Pourcyrous, Massroor Chilakala, Sandeep Elabiad, Mohamad T Parfenova, Helena Leffler, Charles W Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? |
title | Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? |
title_full | Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? |
title_fullStr | Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? |
title_full_unstemmed | Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? |
title_short | Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? |
title_sort | does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets? |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6185793/ https://www.ncbi.nlm.nih.gov/pubmed/29907849 http://dx.doi.org/10.1038/s41390-018-0061-5 |
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